磷酸化

基本解释 (translations)

phosphorylation

与磷酸化相关的网络例句 [注：此内容来源于网络，仅供参考]

CaLP's phosphorylation state analysis of different localization showed that when CaLP is overexpressed alone, it is in state of phosphorylation and stays in the cytoplasm; when CaLP is co-transfected with p21, p21 overexpression causes its unphosphorylation and translocated from cytoplasm to nucleus.

对定位于不同部位的CaLP的磷酸化状态的分析表明：当在细胞中单独表达CaLP时，它以磷酸化形式存在，且磷酸化的位点发生在Y139上，CaLP因此定位于细胞质中；当共表达CaLP与p21时，p21的过表达引起CaLP发生去磷酸化，CaLP由细胞质穿梭入细胞核并与p21发生直接相互作用。

To master the ultrastructure of mitochondrion;the molecular structure elements of Oxidative Phosphorylation;electron-transport chain;the coupling mechanism of Oxidative Phosphorylation and electron transport;the main content of chemiosmotic coupling hypothesis;the structure and chemical composition of thylakoid;electron transport and photophosphorylation;the mechanism of photophosphorylation;the evidence of endosymbiotic theory.

掌握线粒体的超微结构；氧化磷酸化的分子结构基础；电子传递链；氧化磷酸化作用与电子传递的偶联机制；渗透假说的主要内容；类囊体的结构；类囊体的化学组成；电子传递和光合磷酸化；光合磷酸化的作用机制；内共生起源学说的根据。

Enrichment of phosphoproteins and phosphopeptides is a very critical step for MS analysis because of low abundance of phosphoprotein in cells and the suppressive effect from the nonphosphopeptides in protein digestion.

由于磷酸化蛋白在生物体内含量很低，且在质谱分析时易受到非磷酸肽的干扰，因而磷酸肽和磷酸化蛋白质的富集成为磷酸化肽和磷酸化蛋白质分析的一个关键步骤。

If the specific surface area (0.3391 m2/g) of non-modified tea extracted residual was set as 1, the specific surface area of 9 adsorbents, modified with optimized condition, will be 24.7 thiocarbamide plus phosphorylation (1, 12.2 phosphorylation (1, 6.7, 6.5 phosphorylation (2, 6.1 (sodium thiosulfate modification), 5.9 formaldehyde (1, 5.8 formaldehyde (2, 5.4, and 4.9.

设未经修饰过茶叶渣比表面积(0.3391 m2/g)之相对比值为1，其余九种化学修饰化法制备之吸附剂比表面积相对比值分别为硫脲加磷酸化修饰处理法24.7，磷酸化修饰处理法 12.2，磷酸化修饰处理法 6.7，硫脲提升纤维素架桥作用6.5，硫代硫酸钠修饰处理法6.1，甲醛修饰处理法 5.9，甲醛修饰处理法 5.8，醋酸修饰处理法5.4，柠檬酸修饰处理法4.9。

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

An antibody binding to IGF-IR and inhibiting the binding of IGF-I and IGF-II to IGF-IR which is characterized in that said antibody is a is ofIgG1 isotype, b shows a ratio of IC50 values of inhibition of the binding of IGF-I to IGF-IR to the inhibition of binding of IG-II to IGF-IR of 1:3 to 3:1, c inhibits for at least 80% at a concentration of 5 nM IGF-IR phospohrylation in a cellular phosphorylation assay using 3T3 cells providing 400,000 to 600,000 molecules IGF-IR per cell in a medium containing 0.5% heat inactivated fetal calf serum when compared to such an assay without said antibody, and d shows no IGF-IR stimulating activity measured as IGF-IR phophorylation at a concentration of 10 M in a cellular phosphorylation assay using 3T3 providing 400,000 to 600,000 molecules IGF-IR per cell in a medium containing 0,5% heat inactivated fetal calf serum when compared to such an assay without said antibody has improved properties in antitumor therapy.

一种已经提高了抗肿瘤治疗的特性的抗体，所述抗体结合IGF-IR并且抑制IGF-I和IGF-II与IGF-IR结合，其特征在于所述抗体a是IgG1同种型，b显示其对IGF-I与IGF-IR结合的抑制的IC 50 值与其对IGF-II与IGF-IR结合的抑制的IC 50 值的比率为1∶3-3∶1，c当与没有所述抗体的这种测定比较时，其在5nM的浓度上，在包含0.5％的热灭活胎牛血清的培养基中，使用3T3细胞的细胞磷酸化测定中，抑制至少80％的IGF-IR磷酸化，所述3T3细胞提供400，000-600，000分子IGF-IR/细胞，和d当与没有所述抗体的这种测定相比，在包含0.5％的热灭活胎牛血清的培养基中，使用3T3的细胞磷酸化测定中，其在10μM的浓度上没有显示作为IGF-IR磷酸化所测量的IGF-IR刺激活性，所述3T3提供400，000-600，000分子IGF-IR/细胞。

Furthermore, influences of different phosphate salts at various concentrations on the ionization efficiency of phosphopeptide were investigated systematically, finding that the signal intensity for phosphopeptide 48FQEEQQQTEDELQDK63 digested from β-casein were 5 to 8 times increased in an optimized condition with 10 mmol/L ammonium monobasic phosphate or 3 to 4 times increased with 10 mmol/L ammonium dibasic phosphate as additive to matrix 2,5-dihydroxybenzoic acid, respectively.

考察了两种适合于磷酸化肽离子化的基质类型2，5-二羟基苯甲酸和2，4，6-三羟基苯乙酮。用2，5-二羟基苯甲酸作为基质时，当加入10 mM 磷酸氢二铵时，磷酸化蛋白质β-casein的磷酸肽 48FQEEQQQTEDELQDK63的离子化效率可以增强5-8倍，当加入10 mM磷酸二氢胺时，磷酸肽的离子化效率可以增强3-4倍。

These changes were prevented by genistein (a protein tyrosine kinase inhibitor) and antioxidant N-acetyl-L-cysteine, but promoted by sodium orthovanadate (a protein phosphatase inhibitor), which were administered to the SD rats 20 min before ischemia.

进一步的研究表明，缺血前20 min腹腔注射给药，然后缺血30 min，发现蛋白酪氨酸激酶抑制剂染料木黄酮和抗氧化剂N-乙酰半胱氨酸能显著地抑制核内STAT3的磷酸化水平及DNA结合活性的增加(磷酸化水平从2.3和2.5倍分别降为1.2和1.4倍， DNA结合活性则从2.8和3.7倍分别降为1.1和1.5倍)，而蛋白酪氨酸磷酸酶抑制剂矾酸钠则能明显地促进他们的增高(磷酸化水平从2.0倍增到3.4倍， DNA结合活性从3.1倍增为5.1倍)。

Stabilized, hypophosphorylated β-catenin translocates to the nucleus, where it interacts with transcription factors of the TCF/LEF-1 family, leading to the increased expression of genes, such as c-myc and cyclin D1

那么，药物的作用有以下几个可能性：2。药物促进或抑制catenin的核转位，但不影响其磷酸化程度3。药物可直接磷酸化catenin或直接使其去磷酸化，即具有磷酸激酶或磷酸酶的作用。

To prepare the phosphorylated PRAS40 (Ser183) antibody, We chosen 10-amino acid including Ser183 as antigen peptide through antigenicity and hydrophobicity analysis, hinged on keyhole limpet hemocyanin, and used the KLH-peptide to immunize rabbits. After antibody serum titer detection by enzyme linked immunosorbent assay, the antibody was purified with rProtein A sepharose fast flow and dephosphorylated antigen membrane. The antibody titrate reached 1:10 000 after purification and its special property was enhanced with absorption treatment of dephosphorylated antigen membrane. In addition, we used rabbit anti-PRAS40 antibody and the phosphorylated PRAS40 (Ser183) antibody to detect PRAS40 expression in several cell lines, including the normal cells HL7702, HEK293, tumor cells HepG2, A549 and S180. There were no quite difference among these cells; otherwise, we observed the decreased phosphorylation level of Ser183 after amino acid withdrawal treatment.

为了制备PRAS40(Ser183)磷酸化多克隆抗体，本实验通过蛋白疏水性抗原性分析设计多肽抗原，用其免疫家兔获得抗血清， ELISA检测其效价为1：10 000； Western blotting法检测发现，通过rProtein A Sepharose亲和层析纯化并经非磷酸化的抗原条吸附处理后的抗体可以明显提高磷酸化抗体的特异性；用PRAS40抗体及PRAS40(Ser183)磷酸化抗体对正常细胞HL7702、HEK293及肿瘤细胞HepG2、A549、S180的检测显示：磷酸化的Ser183在不同细胞中表达差异不显著，而在经细胞饥饿处理的HEK293细胞中却明显观察到了S183磷酸化水平随氨基酸含量降低而减弱的现象。

与磷酸化相关的网络解释 [注：此内容来源于网络，仅供参考]

glycogen phosphorylase：糖原磷酸化酶

糖原分解第一步是从糖链的非还原端开始,在糖原磷酸化酶(glycogen phosphorylase)作用下分解下1个葡萄糖基,生成1-磷酸葡萄糖,当糖链上的葡萄糖基逐个磷酸解,由于位阻效应,磷酸化酶不能再发挥作用.

oxidative phosphorylation：氧化磷酸化

* 定义 氧化磷酸化 (oxidative phosphorylation)是指在呼吸链电子传递过程中偶联ADP磷酸化,生成ATP,又称为偶联磷酸化. 底物水平磷酸化 (substrate level phosphorylation) 是底物分子内部能量重新分布,生成高能键,使ADP磷酸化生成ATP的过程.

oxidative phosphorylation：藉由电子传递链产生高能磷酸键的磷酸化反应

5. substrate-level phosphorylation: 非电子传递链产生高能磷酸键的磷酸化反... | 6. oxidative phosphorylation: 藉由电子传递链产生高能磷酸键的磷酸化反应 | 7. inner membrane of mitochondria: 电子传递链进 的场...

phosphorylase：磷酸化

早期他们共同研究肝醣磷酸化(phosphorylase)在细胞中是如何被磷酸化时发现,肝醣磷酸化并不是直接被CAMP磷酸化,而是经由另一种激(phosphorylase kinase)来完成,随後他们又发现这种激的活性也受到磷酸化的调控,

phosphorylase：磷酸化酶[如磷酸化酶a、b等]

phosphorus pentoxide 五氧化二磷 | phosphorylase 磷酸化酶[如磷酸化酶a、b等] | phosphorylase kinase 磷酸化酶激酶

sucrose phosphorylase：蔗糖磷酸化酶

其反应如下:(1)蔗糖磷酸化酶(sucrose phosphorylase)途径 这是微生物中蔗糖合成的途径. 1943年Doudoroff等在假单胞菌(Pseuomonas saccharophila)的细胞中提取得到蔗糖磷酸化酶,当有无机酸的存在时,可以将蔗糖分解为1-磷酸葡萄糖和果糖,

phosphorylase kinase：磷酸化酶激酶

phosphorylase 磷酸化酶[如磷酸化酶a、b等] | phosphorylase kinase 磷酸化酶激酶 | phosphorylated linker 磷酸化接头

substrate-level phosphorylation：非电子传递链产生高能磷酸键的磷酸化反应

4. citric acid cycle: 解作用后进 有氧呼吸的重要反应 | 5. substrate-level phosphorylation: 非电子传递链产生高能磷酸键的磷酸化反应 | 6. oxidative phosphorylation: 藉由电子传递链产生高能磷酸键的磷酸化反...

cyclic phosphorylation：循环磷酸化; 循环磷酸化作用

循环 circulation | 循环磷酸化; 循环磷酸化作用 cyclic phosphorylation | 循环系统 circulatory system

distarch phosphate phosphated：磷酸化磷酸双淀粉

distarch phosphate acetylated 磷酸乙酰双淀粉 | distarch phosphate phosphated 磷酸化磷酸双淀粉 | distasteful 讨厌的口味;不愉快的口味